MicroRNA-24 regulates apoptosis of cardiomyocytes after myocardial infarction

AIM：To evaluate the expression of miR-24 in infarcted myocardial tissues and to investigate the function of miR-24 during cardiomyocyte apoptosis in vitro and in vivo. METHODS：The mouse model of myocardial infarcton (MI) was established. The expression of miR-24 in the sections of infarcted myocardial tissues was measured by qRT-PCR. The expression of miR-24 was modified by transfecting oligonucleotide mimic and inhibitor of miR-24 into cardiomyocytes, or injecting lentiviral vectors intramyocardially. The apoptosis of cardiomyocytes was detected by Caspase-Glo 3/7 Assay System. The heart functions were determined by echocardiography and the scar size in MI model was observed with Masson trichrome staining. The apoptosis of infarcted myocardial tissues was detected by TUNEL method. Microarray and bioinformatic analysis were also used to predict the targets of miR-24. RESULTS：The expression of miR-24 in the infarct and border areas was down-regulated after MI. Overexpression of miR-24 in cardiomyocytes reduced the apoptosis induced by hypoxia. miR-24 transfection resulted in reduction of the scar size, and improved left ventricular fractional shortening (LVFS) and left ventricular ejection fraction (LVEF) of the mice in treatment group after 2 weeks. Furthermore, miR-24 reduced cell apoptosis in the infarct region. BCL2L11, ANK3 and SGPL1 may be the targets of miR-24 during the process of anti-apoptosis. CONCLUSION：miR-24 is down-regulated in the infarcted myocardial tissues. In vitro, miR-24 reduces apoptosis of cardiomyocytes induced by hypoxia. In vivo, miR-24 attenuates cell apoptosis in the infarct and border areas of the heart 2 weeks after MI, and ultimately improves heart functions.